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Phase 2A > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are endocrine hormones?

A

blood borne, acting at distant sites

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2
Q

What are exocrine hormones?

A

glands that pour secretions through a duct to the site of action

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3
Q

What are paracrine hormones?

A

hormones acting on adjacent cells

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4
Q

What are autocrine hormones?

A

Feedback on the same cells that secretes the hormone

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5
Q

Water soluble hormones
how is it transported, interacts with cell, half life, clearance, ex?

A

unbound, binds to surface receptor, short HL, fast clearance, peptides / monoamines

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6
Q

Fat soluble hormones
how is it transported, interacts with cell, half life, clearance, ex?

A

Protein bound, diffuses into the cell, long HL, slow, thyroid hormones, steroids

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7
Q

Name the 4 hormone classes?

A

peptides, amines, iodothyronine, steroids

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8
Q

Nature of peptides as hormones & ex?

A

linear / ring / vary in length
ex insulin

  • stored in secretory granules
  • released in pulses or bursts
  • cleared by tissue or circulating enzymes
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9
Q

Nature of amines as hormones & ex?

A

ex adrenaline & noradrenaline

  • water soluble
  • binds to alpha & beta adrenoreceptors
  • stored in secretory granules
  • released in pulses or bursts
  • rapid clearace
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10
Q

Nature of iodothyronine as hormones & ex?

A

thyrosine, iodine

  • basis of thyroid hormone synthesis
  • not water soluble, 99% protein bound
  • usually measure T3 & T4 not this
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11
Q

How might iodothyronine be synthesised into thyroid hormones?

A
  • thyroglobulin released into colloid - acts as base for thyroid hormone synthesis
  • iodine + tyrosine → iodothyrosine
  • conjugation of iodothyrosines give rise to T3 & T4 & stored in colloid bound to thyroglobulin
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12
Q

Subtypes of steroids & cholesterol derivatives?

A

vitamin D, adrenocortical & gonadal steroids, steroid

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13
Q

Nature of vitamin D?

A

it is a hormone!!

  • fat soluble
  • enters cell directly to nucleus to stimulate mRNA production
  • Transported by vitamin D binding protein
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14
Q

Nature of adrenocortical & gonadal steroids?

A
  • protein bound - fat soluble
  • usually bind to cytoplasmic receptor, pass to nucleus and induce a response
  • altered to active metabolites
  • inactivated in liver by reduction and oxidation or conjugation to glucoronide & sulphate groups
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15
Q

Nature of pure steroids?

A
  • diffuse through plasma membrane (lipid soluble!), binds to receptor
  • binding occurs in cytoplasm, move to nucleus
    • mimic transcription to form mRNA → exert steroid function
    • (protein synthesis?)
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16
Q

Where are hormone receptors found and what type of hormones bind to them respectively?

A
  1. Cell Membrane (peptide)
  2. Cytoplasm (steroids)
  3. Nucleus (thyroid, estrogen, vitamin D)

think about fat solubility!

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17
Q

Types of hormone secretion patterns?

A

continuous or pulsatile

superadded rhythms - day/night cycles

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18
Q

Define type 1 diabetes mellitus?

A

autoimmune condition where beta cells are damaged with genetic component

profound insulin deficiency

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19
Q

Define type 2 diabetes mellitus?

A

chronic hyperglycaemia due to relative insulin deficiency, resistance or both

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20
Q

Diagnostic criteria for DM!

A
  • HbA1c ≥ 48 mmol / mol (6.5%)
  • Fasting VBG ≥ 7 mmol/L
  • Random VBG ≥ 11.1 mmol/L
  • OG Tolerance T>11 mmol/L
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21
Q

If someone is prediabetic, they would have

A

Impaired glucose tolerance

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22
Q

Where is insulin produced?

A

pancreas

Beta cells in the pancreatic islet of Langerhans

INHIBITED by beta blockers

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23
Q

How does insulin work?

A

acts on the liver to reduce its glucose output, inhibiting glycogenolysis and gluconeogenesis

promotion of glucose uptake in peripheral tissues

Decreases serum potassium through stimulation of Na/K ATPase pump

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24
Q

Risk factors for type 1

A
  • Northern European / Scandinavian
  • Family History (less but is)
  • Other autoimmune disease as comorbidity
    • Addison’s, coeliac, autoimmune thyroid
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25
Q

Risk factos for type 2

A
  • sedentary lifestyle, diet high in calories, obseogenic environment
  • overweight
  • fam hx - gestational diabetes, hypertension / vascular disease
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26
Q

Pathophysio of type 1?

A

autoimmune

pancreas stops producing insulin. glucose is not taken up

level of glucose in blood keeps rising → hyperglycaemia

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27
Q

Pathophysio type 2?

A
  • repeated exposure to glucose & insulin makes cells in the body resistant to insulin
  • beta cells in pancreas fatigued & damaged therefore producing less
  • or due to lipid depo in pancreatic islets, normal secretion cannot be
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28
Q

Differentiate type 1 / type 2 DM?

A

ketones
1 - increasing level // 2 - almost never excess

insulin
1 - deficiency // 2 - always detectable

both lead to profound skeletal muscle breakdown & unrestrained lipolysis

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29
Q

Presentations - T1DM?

A

4T’s: toilet, thin, tired, thirsty

  • Short history, rapid onset
  • Weight loss, fatigue → check if intentional
    • lipid & muscle loss due to unrestrained gluconeogenesis
  • Repeated infections? Blurred vision?
  • Moderate or large urinary ketones
  • immediate tx with insulin!
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30
Q

Additional testing for type 1?

A

for other autoimmune diseases

and for antibodies related to T1DM

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31
Q

Antibodies associated with T1DM?

A
  • Anti GAD
  • Pancreatic islet cell antibodies
  • Islet antigen-2 antibodies
  • ZnT8

common in children, the more the better

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32
Q

Presentations - T2DM?

A
  • Usually in people over 30’s
    • More obese children
    • and obese now?
  • Onset is very gradual
  • Stronger positive family history
    • (less in type 1!!)
    • identical twins, almost 100% concordance
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33
Q

Further typical presentations, T2DM

(like if you misdiagnosed and seeing patient again…)

A

ketone breath

free fatty acid from impaired glucose uptake - lipolysis instead so produces ketone bodies

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34
Q

Differentiate T1 & T2 at presentation?

A

type 2 in younger, including childhood

but t1 can be obese, uncontrolled t2 can present with weight loss & ketonuria → check hx, weight loss intentional?

if in doubt treat with insulin

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35
Q

Goal of treatment - DM

A

if not on insulin = normal HbA1c 50 mmol/mol

if on insulin = fasting BG between 4-7mmol/L

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36
Q

Types of insulin & how they should be used?

A

basal Insulin - covers time between meals and especially during the night, given once or twice daily

prandial or bolus (meal time) insulin (rapid acting analogues) → adjusted according to glucose & carbohydrate content of meals

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37
Q

Typical insulin regime for type 1?

A

intensive basal-bolus (both types) used = best treatment

separate basal from bolus to mimic physiology

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38
Q

Typical insulin regime for type 2?

A

insulin usually given later on in disease course, or those with poor glycemic controls

usually start with just basal → lowers nocturnal, may add bolus later (and is often required)

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39
Q

Ways insulin can be given (dosage)?

A
  • analogue insulin - less risk of hypoglycemia
  • premix insulin - (mixed quick acting & long acting) - better for people who don’t want to take 5 injections a day
    • but risks of hyper / hypo as day goes by and higher target needed
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40
Q

GUIDELINE order for oral therapy T2DM
[2022]

A
  1. metformin / metformin MR (Gi into)
    if CVD with SGLT2 inhibitors
  2. DPP4 inhibitor / pioglitazone / sulfonylurea
  3. insulin and/or GLP-1
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41
Q

Mechanism of metformin?

A
  • decrease hepatic glucose output (gluconeogenesis) & increase peripheral glucose uptake (+ insulin sensitivity!)
  • AMP kinase activation - helps with weight loss
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42
Q

Metformin CI?

A

CA renal and hepatic impairment, reduce dose or avoid

acute alcohol intox & chronic alcohol abuse

withheld 48 hours after injecting IV contrast media (+ renal imapirment)

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43
Q

Metformin SE?

A

biggest is lactic acidosis & GI upset

anorexia / diarr / nausea / abdo pain

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44
Q

Mechanism of SGLT-2 inhibitors

(‘flozin’s)

A
  • block the reabsorption of glucose in the kidney, increase glucose excretion & lower blood glucose levels
  • also helps with weight loss
  • Specific benefit in reducing CV mortality!
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45
Q

Examples of SGLT-2 inhibitors?

A

‘flozin’s

Empaglifozin, Dapaglifozin, Canaglifozin, Ertugliflozin

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46
Q

CI SGLT-2 inhibitors?

A

CI ketoacidosis

CA in renal impairment, diuretics, low systolic BP & elderly

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47
Q

SE SGLT-2 inhibitors?

A

genital thrush

increased risk of euglycaemic ketoacidosis in T2

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48
Q

Incretins - what are they?

A

GLP-1 & GIP - glucose dependent, released by intestines to food, inactivated by DPP-4!

promote insulin secretion & suppress glucagon release

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49
Q

Mechanism of DPP-4 inhibitors

(‘gliptin’s)

A

lowers blood glucose by competitively inhibiting the action of DPP-4 (enzyme) which destroys incretins

low risk of hypo, no effect on weight

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50
Q

Examples of DPP-4 inhibitors?

A

vidagliptin, sitagliptin

‘gliptin’s

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51
Q

CI DPP-4 inhibitors?

A

type 1, ketoacidosis

preg, breastfeed, elderly >80, pancreatitis

moederate to severe renal impairment

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52
Q

SE DPP-4 inhibitors?

A

low risk, but still present, of hypoglycaemia

acute pancreatitis

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53
Q

Which type of medications may mask symptoms of hypoglycaemia?

A

beta blockers

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54
Q

Mechanism of pioglitazone?

A

improve insulin sensitivity, binds to peroxisome proliferator activated receptor

activate genes concerned with glucose uptake, utilisation & metabolism

→ need insulin for a therapeutic effect, so relatively rarely used

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55
Q

CI pioglitazone?

A

heart failure, macular haem or oedema, high risk of fractures

avoid in hepatic impairment

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56
Q

Mechanism of sulfonylureas?

A
  • stimulate pancreatic insulin release by binding to beta cell receptors
  • improve glycemic control, but at the expense of weight fain
  • can cause hypo

→ only in patients with residual pancreatic function

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57
Q

CI & SE sulphonylureas?

A

renal & hepatic impairment

GI upset, hypoglycaemia

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58
Q

Complications for diabetes?

A

Retinopathy, nephorpathy, neuropathy

cardiovascular disease

acidosis

hypoglycaemia

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59
Q

Feature of diabetic ketoacidosis?

A

Must have all 3!!

  • Hyperglycaemia: plasma gluc > 50 mmol / l
  • Raised plasma / urinary ketones: 3mmol/L or > 2+ dipstick
  • Metabolic acidosis plasma bicarbonate bicarbonate < 15.0 mmol/L and/or venous pH < 7.3
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60
Q

Which type of DM is more prone to DKA?

A

type 1 (lots of ketones)

but type 2 incidences increasingly recognised - as low insulin levels are sufficient to suppress catabolism & prevent ketogenesis, but may occur when hormone rise to high lvl, e.g MI

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61
Q

How can ketones cause acidosis?

A

Lack of insulin = unable to utilise glucose

Lipolysis instead: products = ketones (acetone, beta-hydroxybutyrate and acetoacetate) → acidic

accumulates in blood = acidosis

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62
Q

Present - ketoacidosis

A

Hyperventilation - getting rid of Co2 & carbonic acid in blood

dehydration - might pres with vomit / diarr, hypotention, tachycardia, coma

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63
Q

Treatment of ketoacidosis?

A

1st line - rehydration, 3l first 3 hours
20ml /kg 0.9% NaCl over 15 mins
replace slowly or risk of cerebral oedema

insulin - reverse ketone production & fat breakdown

replace electrolytes, esp K+ (drive in to cell)

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64
Q

Complications DKA?

A

Cerebral oedema = swelling of brain parenchyma

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65
Q

What are the counterregulatory hormones for insulin?

A

glucagon, adrenaline, cortisol, growth hormone

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66
Q

When might someone be at risk for hypoglycaemia?

A
  • Low HbA1c, High pre-treatment HbA1c in type 2
  • long duration of diabetes
  • daily insulin dosage > 0.85 U / kg / day
  • history of previous hypo, recent episodes of severe hypo
  • impaired awareness → checks if ability to secrete adrenaline is still intact
    • → ask when do they get hypo symptoms! if below 3.0 mmol / l = adrenaline no longer exists, if above = adrenaline still there
  • physically active
  • impaired renal and or liver function
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67
Q

Hypoglycaemia - symptoms?

A

Autonomic: trembling, palpitations, sweating, anxiety, hunger

Neuroglycopenic: difficulty concentrating, confusion, weakness, drowsy / dizziness, vision changes & difficulty speaking

Non-specific: nausea & headache

** may be symptomless if adrenaline secretion is gone too (beta blocker!)

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68
Q

Diagnostic criteria for hypoglycaemia?

A

If no known DM then Whipple’s triad

  • blood glucose concentration < 4.0 mmol/L
  • symptoms of hypoglycaemia
  • Reversal of symptoms when BG normal
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69
Q

Which other conditions can cause hypoglycaemia?

A
  • Beta cell secretagogue ingestion (e.g. ingestion of a medication that stimulates insulin release from beta cells)
  • Islet beta-cell tumour (e.g. insulinoma)
  • Functional beta cell disorder (e.g. high insulin secretion not due to an insulinoma)
  • Insulin autoimmune hypoglycaemia (antibodies develop against insulin or its receptor)
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70
Q

Treatment for hypoglycaemia?

A
  • glucose load - oral if alert, IV if coma
  • retest and give more if needed
  • if coma does not respond - consider glucagon but diff if poor glycogen stores; then IV glucose infusion if needed
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71
Q

How might one prevent hypoglycaemia?

A
  • correct choice of therapy - sulfonylureas and insulin
  • adjust targets, specialist support?
  • discuss with patient - alcohol, exercise, consider sleep & age
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72
Q

What is diabetic neuropathy?

A

a collection of conditions that result from glucose-related damage to neurones of the somatic and autonomic nervous systems

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73
Q

Signs and symptoms, diabetic neuropathy?

A

glove and stocking sensory loss

Pain - burning, nocturnal exacerbation
like electrical shocks, walking on glass

Extreme spectrum sensitivity - hyper & paraesthesia, insensitivity

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74
Q

Consequences of diabetic neuropathy?

A

Diabetic foot ulceration, Charcot’s joint

Peripheral neuropathy & peripheral vascular disease - nerves and circulation affected and damaged

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75
Q

Treatment for general diabetic neuropathy?

A

good glycaemic control

opioids, antidepressants etc,

Transcutaneous nerve stimulation / acupuncture / spinal cord stimulators / Psychological interventions

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76
Q

Screening tests for diabetic foot ulceration?

A
  • Test sensation
    • 10 gm monofilament
    • neurotips
  • Vibration perception
    • tuning fork
    • biothesiometer
  • Ankle reflexes
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77
Q

Treatment for diabetic foot ulceration?

A

lower limb amputation

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78
Q

What is diabetic retinopathy?

A

Persistent damage to retina leads to ischaemia and angiogenic factors which promotes new formation of weak and friable vessels → microaneurysms, haemorrhage, fibrosis retinal detachment

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79
Q

Risk factors for diabetic retinopathy?

A
  • long duration diabetes
  • poor glycemic control
  • hypertensive
  • on insulin treatment
  • pregnancy
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80
Q

How might one prevent diabetic retinopathy?

A

National Eye screening programme

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81
Q

Treatment for diabetic retinopathy?

A
  • Laser therapy
    • proven treatment for DR
    • aim is to stabilise changes
    • but treatment does not improve sight!!
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82
Q

What is diabetic nephropathy & pathophysiology?

A

Diabetic kidney disease

High BG → damage to blood vessel clusters in kidney & kidney itself → pressure increased on filtering system in the kidneys → glomerular changes/injury → filtration rate endangered → DN

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83
Q

Present diabetic nephropathy?

A

hallmark = proteinuria (albuminuria)

reduced calculated creatinine clearance, decreased glomerular filtration rate

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84
Q

How might one screen for diabetic nephropathy?

A

at least two urine samples, collected with 3-6 months

test for urine albumin, albumin:creatine ratio, eGFR

→ can use CKD classify system

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85
Q

Consequences / complications - diabetic nephropathy?

A

major risk for CVD, kidney failure

this is more common in T2 and less in T1

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86
Q

What is peripheral vascular disease?

A

decreased perfusion to an area due to macrovascular disease

symptoms more likely to occur at more dital sites

= 15-40x more likely for amputation

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87
Q

Signs and symptoms of peripheral vascular disease?

A

most common at more distal sites

intermittent claudication + rest pain = key

  • Diminished or absent pedal pulses
  • Coolness of feet and toes
  • Poor skin & nails
  • Absence of hair on feet & legs
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88
Q

How might one diagnose peripheral vascular disease?

A

Doppler Pressure studies & Ankle Brachial Index!

Duplex arterial imaging / MRA

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89
Q

Treatment for peripheral vascular disease?

A
  • quit smoking
  • Pressure relieving footwear, podiatry, revascularisation, antibiotics
  • surgical intervention
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90
Q

Preventive measures for peripheral vascular disease (& diabetic foot)?

A
  • Screening
  • Education, providing orthotic shoes
  • MDT Foot clinic - treat the ulcer !!!!
  • Pressure relieving footwear, podiatry, revascularisation, antibiotics
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91
Q

Which hormones are released by the anterior pituitary?

A
  • Thyroid stimulating hormone (TSH) → Thyroid
  • Adrenocorticotropic hormone (ACTH) → Adrenal cortex
  • Follicle stimulating hormone (FSH) & Luteinising hormone (LH)
  • Growth hormone (GH) → entire body & liver
  • Prolactin → Mammary gland
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92
Q

Which hormones are released by the posterior pituitary?

A

Oxytocin, Antidiuretic Hormone (ADH)

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93
Q

Outline the thyroid axis?

A

= Hypothalamus stimulating (via anterior pituitary) thyroid, releases T3 & T4

  1. Hypothalamus: Thyrotropin-releasing hormone (TRH)
  2. Anterior Pituitary: Thyroid stimulating hormone (TSH)
  3. Thyroid: triiodothyronine (T3) & Thyroxine (T4)

= Negative feedback cycle to control hormones

  1. Hypo & AP: senses T3 & T4: Suppress TRH & TSH
  2. Lower amount of T3 & T4 released
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94
Q

Function of thyroid hormones?

A
  • accelerates and enhances food metabolism
  • increase ventilation, heart rate & cardiac output
  • growth rate accelerated & brain dev postnatal
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95
Q

How is thyroid hormone consumed by the body?

A

Thyroid gland produces thyroxine (T4) which is converted to triiodothyroxine (T3) in target tissues!

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96
Q

What is primary hyperthyroidism?

A

thyroid pathology → excessive Thyroid hormone

pathology = thyroid

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97
Q

Causes for primary hyperthyroidism?

A
  • graves’ disease (75-80%)
  • toxic multinodular goitre
  • toxic adenoma
  • drug induced - AMIODARONE (high iodine)
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98
Q

What is secondary hyperthyroidism?

A

thyroid overstimulated by thyroid stimulating hormone → excessive TH

pathology = hypothalamus or pituitary

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99
Q

What is Grave’s disease?

A

TSH receptor antibodies (abnormal) produced by immune system mimics TSH, overstimulate TSH receptors on thyroid → excessive TH

pathology = autoimmune

→ associated with anti-TSH antibodies and anti-thyroglobulin (anti-tg)

→ may cross placenta! ophthalmopathy strongly associated

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100
Q

What is a goitre?

A

palpable & visible thyroid enlargement

  • variety of causes
  • commonly sporadic or autoimmune
  • endemic in iodine deficient areas
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101
Q

3 mechanisms for increased levels of thyroid hormones (T3 or T4)?

A
  • overproduction of thyroid hormones
  • leakage of preformed hormone from (inflamed) thyroid
  • ingestion of excess thyroid hormone (from overtreatment or overingestion of pharm)
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102
Q

General symptoms of hyperthyroidism?

A

Goitre - may develop into facial swelling

  • tachycardia
  • lid-lag + stare → suspect autoimmune
  • anxiety, irritability, sweating, heat intolerance
  • Unintentional weight loss but with increased appetite, diarrhoea
  • frequent loose stools
  • Sexual dysfunction, sub-fertility, menstrual disturbance (infrequent & light)
  • dry, brittle hair or thinning hair on your scalp and body - underactive thyroid
  • AF lol
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103
Q

Grave’s specific symptoms of hyperthyroidism?

A
  • Diffused goitre - symmetrical
    • entire, smooth
  • Pretibial myxoedema - waxy oedematous on tibia - specific to Grave’s
  • Thyroid eye disease - 50% - eyes & eyelids are swollen and red
  • Exophthalmos - bulging of the eyeball out of the socket (stare-y eyes) (from swelling, inflam & hypertrophy of tissues behind eyes)
  • Acropachy - finger clubbing
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104
Q

Differentiate between a diffused goitre vs a nodular goitre?

A

Diffused - entire thyroid gland swells and feels smooth to the touch

Nodular - lumpy to touch due to solid or fluid filled lumps

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105
Q

Biggest risk factor for autoimmune hyperthyroidism?

A

(single biggest) being female → very common postpartum

  • during pregnancy: autoimmune activity goes down
  • postpartum: rise in immunity
    • autoimmune thyroiditis
    • grave’s thyroiditis
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106
Q

Diseases associated with thyroid autoimmunity?

A
  • T1DM
  • Pernicious anaemia
  • Vitiligo (skin discolouration
  • Coeliac disease (1 in 3 with autoimmune hyperthyroidism have coeliac)
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107
Q

Testing for thyroid diseases?

A
  • *Thyroid function tests: free TSH & fT4/T3**
  • *primary** = suppressed TSH
  • *secondary** = inapp high TSH

Thyroid antibodies & isotope uptake scan

urinary iodine secretion

Doppler ultrasound of thyroid for nodules etc

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108
Q

Pharmacological tx for hyperthyroidism?

A

Antithyroid drugs - for symptom control
= act as a preferred substrate for iodination by thyroid peroxidase (key enzyme in thyroid hormone production)

In order - Carbimazole, PTU, beta blockers

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109
Q

Carbimazole - mechanism

A

prevents thyroid peroxidase enzyme (TPO) from coupling and iodinating thyroglobulin (which degrades into T3 and T4) hence reducing production of TPO

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110
Q

Carbimazole indications & regime?

A

1st line, Successful even for Grave’s

Normal thyroid function in 4-8 weeks, may serve as maintenance

Give as either

  • Titration-block: dose is carefully titrated to maintain normal levels
  • Block and replace: dose is sufficient and block all production → patient takes levothroxine titrated to effect
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111
Q

Propylthiouracil PTU mechanism and indications?

A

if carbi not tolerated, prepreg / 1st trimester, specialist for thyroid crisis

inhibits conversion of T4 → T3

small risk of liver injury so not 1st line

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112
Q

How might beta blockers be useful in hyperthyroidism?

A

blocks adrenaline related syndromes of hyperthyroidism = controls symptoms whilst the definitive treatment takes time to work

= propanolol = good choice, as non selective
= very useful in thyroid storm

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113
Q

SE antithyroid drugs?

A

common = rash

less common = arthralgia, hepatitis, neuritis, thrombocytopenia, vasculitis etc
but resolvable if stop drug

agranulocytosis → most serious!!

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114
Q

Signs of agranulocytosis
& how to prevent?

A
  • sore throat, fever, mouth ulcers
  • MUST warn patient before starting ATD
  • STOP if patients develop symptoms & check FBC
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115
Q

Other tx options for hyperthyroidism?

A

radioactive iodine treatment

thyroid surgery

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116
Q

Mechanism for radioactive iodine treatment & indications?

A

1st line definitive for Grave’s & toxic multi-nodular goitre

Uses iodine isotope (as iodine needed for TSH production) to induces DNA damage → death of thyroid cells, causing a decrease in thyroid function and / or reduction in thyroid size

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117
Q

Care & CI, radioactive iodine treatment for hyperthyroidism?

A

radioprotection after treatment - children & preggers

CI Grave’s with active orbitopathy, pregnant / conceiving / breastfeeding women

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118
Q

Thyroid surgery - indications?

A

total or hemi or for single thyroid nodule

for intolerant to drug, recurrence, coexisting potential malignant, compression symp’s

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119
Q

What is Sporadic Non-toxic Goitre

A
  • commonest endocrine disorder
  • 8.6% prevalence thyroid enlargement
  • Euthyroid → thyroid function is normal
  • Goitre - diffuse, multinodular, solitary nodule, dominant nodule
  • differentiate benign from malignant
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120
Q

What is toxic multi-nodular goitre?

A

= Plummer’s disease

nodules develop on the thyroid gland that acts independently of the normal feedback system

continuous production of excessive TSH

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121
Q

Features of toxic multi-nodular goitre?

A
  • goitre with firm nodules
  • Most patient’s aged over 50
  • second most common cause of thyrotoxicosis (hyperthyroidism)
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122
Q

What is De Quervain’s thyroiditis?

A

= Subacute thyroiditis

self limiting condition from viral infection

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123
Q

Features of Subacute thyroiditis?

A

Viral infection with fever, neck pain, dysphagia (swallowing problems)

Features of hyperthyroidism

Phases: viral infect - hyperthyroid - hypothyroid - euthyroid (normal!)

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124
Q

Treatment for De Quervain’s thyroiditis?

A

self limiting

but can treat with NSAIDs for pain & inflam.
beta blockers for symptomatic relief of hyperthyroidism

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125
Q

What is a thyroid storm?

A

emergency, thyrotoxic crisis

rare presentation of hyperthyroidism

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126
Q

Features of a thyroid storm?

A

hyperthermia, tachycardia, arrhythmias, nausea, vomiting, seizures and cognitive decline.

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127
Q

Treatment for thyroid storm?

A

Admission, support with fluid

Pharm
Beta blockers, thionamides (PTU), steroids, Lugol’s iodine

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128
Q

Hypothyroidism - define & types?

A

inadequately low output of thyroid hormones by the thyroid gland

Primary (thyroid pathology) or Secondary (pituitary pathology)

tingling of carpal tunnels

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129
Q

Features of primary hypothyroidism?

A

= 99% hypothyroidism
caused by thyroid gland insufficiency

T3 & T4 will be low
TSH will be high
(pit producing TSH to stimulate thyroid)

130
Q

Features of secondary hypothyroidism?

A

caused by pituitary (or hypothalamic pathology)

TSH will be low → no production

131
Q

How might you investigate hypothyroidism?

A

TSH = most sensitive marker
free T4 to confirm

antibodies - anti-TPO, anti-Tg, TSHR-Ab

132
Q

What is Hashimoto’s thyroiditis?

A
  • autoimmune inflammation of the thyroid gland
  • associated with antithyroid peroxidase (anti-TPO - specific) & antithyroglobulin (anti-tg) antibodies (also in Graves)
  • Goitre → atrophy (shrinkage) of the thyroid gland
133
Q

Causes of primary hypothyroidism?

A

Hashimoto’s thyroiditis

iodine deficiency

tx for hyperthyroidism

medications - lithium & amiodarone
limits production of TSH, interfere with thyroid metabolism

134
Q

Causes of secondary hypothyroidism?

A

hypopituitarism

may be caused by tumours, infection, vascular, radiation

135
Q

Signs and symptoms, hypothyroidism?

A
  • weight gain, fatigue
  • dry skin
  • coarse hair and hair loss
  • fluid retention (oedema, pleural effusions, ascites)
  • heavy or irregular periods
  • constipation
  • muscle - delayed reflexes, cramps
136
Q

Tx for hypothyroidism?

A

Thyroid hormone replacement

oral levothyroxine = T4,
leothyroxine = T3 = shorter half life so for emergency

137
Q

CI thyroid hormone replacements?

A

coronary heart disease, hypopituitarism

138
Q

Interactions for thyroid hormone replacements?

A

increase dose if taking CYP450 inducers e.g. carbamazepine

can increase effects of insulin & warfarin

139
Q

What is the adrenal axis?

A

Hypothalamus stimulating (via anterior pituitary) the adrenal glands (above each kidney), releasing cortisol

140
Q

Effect of cortisol?

A

major metabolic & stress hormone
diurnal variation

  • inhibits immune system & bone formation
  • raises blood glucose
  • increases alertness & metabolism
141
Q

Briefly outline the adrenal axis?

A
  1. Hypothalamus: corticotrophin release hormone (CRH)
  2. Anterior pituitary: adrenocorticotrophic hormone (ACTH)
  3. Adrenal gland: cortisol

= Negative feedback cycle to control hormones

Hypo & AP senses cortisol: suppress release of CRH & ACTH

142
Q

What is Cushing’s - differentiate between syndrome & disease?

A

Syndrome = symptoms that develop after prolonged abnormal elevation of cortisol

Disease = specific condition with excess glucocorticoids resulting from inappropriate ACTH secretion from a pituitary adenoma

→ Disease causes syndrome, but syndrome is not always caused by disease

143
Q

Where is cortisol released from and by?

A

zona glomerulosa of the adrenal cortex above the kidneys

144
Q

3 mechanisms which will give you excess cortisol?

A

either result from excess ACTH (antpit) or from neoplasms in adrenals stimulating z.reticu to release more

also from ingesting excess glucocorticoids, e.g. prednisolone

145
Q

Symptoms, cushing’s

A

= round in the middle (trunk, abdomen and neck) with thin limbs!

  • round ‘moon’ face
  • central obesity
  • abdominal striae
  • buffalo hump = neck
  • osteoporosis
  • easy bruising and poor skin healing
  • failure for children to grow tall despite excess weight
146
Q

Signs of cushing’s

A

High level of stress hormone

  • hypertension
  • cardiac hypertrophy
  • hyperglycaemia (DM2)
  • depression, mood change - irritability
  • proximal weakness
  • gonadal dysfunction
147
Q

Causes of Cushing’s

A
  • pituitary adenoma releasing excess ACTH (can be benign), peak 30-50 yrs
  • adrenal adenoma = 80%
  • ectopic ACTH = small cell lung cancer / carcinoid tumours
  • exogenous steroids - long term high dose
  • alcohol pseudo-Cushing’s, obese, preg
148
Q

Differentials - Cushing’s

A
  • alcohol pseudo-Cushing’s = caused by alcohol excess, resolve 1-3 wks after abstinence
  • asthma patients on ACTH
  • obesity, pregnancy
149
Q

How might you investigate Cushing’s

A

Dexamethasone suppression test, 24hr & 48 hr, if positive then

plasma ACTH, if positive then

High dose dexameth supp / corticotropin releasing hormone (CRH) test

150
Q

Outline Dexamethasone Suppression Test?

A

should in a healthy patient, send neg feedback to pit&hypo → decreased ACTH & cortisol

low dose given to patient at midnight & cotisol & ACTH measured in the morning

if cortisol suppression < 50nmol, then Cushing’s can be excluded

high / normal cortisol = further invest for type

151
Q

How might high dose dexamethasone suppression test differentiate between diff types of abnormalities

A

High dose = 8mg = further invest

Cushing’s = cortisol suppressed

Adrenal adenoma = cortisol unsuppressed, ACTH suppressed

Ectopic ACTH = neither cortisol nor ACTH suppressed

152
Q

How might a 48h dexamethasone confirm the diagnosis?

A

Oral dex x4/day for 2 days, measure cortisol at 0 & 48hr

in Cushing’s there will be no suppression of cortisol

153
Q

If dex suppression tests are positive, how might you further confirm diagnosis of Cushing’s?

A

Plasma ACTH

if ACTH detectable then distinguish pituitary cause from ectopic ACTH production → high dose dexa or CRH test

if ACTH undetectable then adrenal tumour. Image to confirm; if no mass then adrenal vein sampling

154
Q

What is a Corticotropin releasing hormone (CRH) test?

A
  • Human IV CRH given - activates and release ACTH
  • Measure cortisol at 120 mins
  • Cortisol will rise with pituitary disease but NOT with ectopic ACTH production
  • if positive cortisol response to CRH → cushing’s disease, pit MRI to confirm
  • if negative cortisol response to CR → hunt for ectopic source of ACTH
155
Q

Alternative to dexamethasone test?

A

24 hour urinary free cortisol

but cumbersome to carry out and does not indicate underlying cause

Take > 2 measurements (cortisol is bound to albumin, when capacity is reached then will spill out to urine)

156
Q

Tx for Cushing’s?

A

Surgical & pharma to inhibit cortisone synthesis

157
Q

Surgical options for Cushing’s?

A

remove pituitary adenoma
go with trans sphenoidal

if impossible or adrenal adenoma
bilateral adrenalectomy & replacement hormones for life

if adrenal carcinoma = radiotherapy & adsrenolytic drugs - e.g. mitotane

158
Q

If source unlocatable or recurrence post op - syndrome?
present?

A

Nelson’s syndrome

present as increased skin pigmentation from enlarged pit tumour

will respond to pit radiotherapy

159
Q

Pharma options for Cushing’s

A

Drugs to inhibit cortisol synthesi
esp ectopic ACTH, post op or awaiting radiation

= METYRAPONE, KETOCONAZOLE and FLUCONAZOLE

160
Q

What is acromegaly

A

multi-system disorder characterised by excessive growth hormone

mean age of diag = 44!

161
Q

Cause of acromegaly?

A

benign pituitary GH producing adenoma
in almost all cases

expansion of the tumour in the pituitary can result in compression of surrounding structures resulting in headaches & visual field loss

hyperplasia e.g. ectopic GH releasing hormone from a carcinoid tumour
in rare cases

162
Q

Action of growth hormone?

A
  • indirectly through induction of insulin-like growth factor (IGF-I) which is synthesised in the liver & other tissues
  • directly onto tissues such as the liver, muscle bone, or fat to induce metabolic changes
163
Q

GH secretion monitoring?
inhibited by? stimulated by?

A

inhibited by somatostatin & high glucose!

stimulated by ghrelin - synthesised in stomach, also stimulates GH secretion

164
Q

Classification of acromegaly?

A
  • gigantism = excessive GH production in children before fusion of the epiphytes of the long bones
  • acromegaly = excess GH in adults
165
Q

Presentation - acromegaly?

A
  • large hands = ‘acral enlargement’ - tight rings, carpal tunnel in 50%
  • maxillofacial changes
    • coarsening of facial features
    • wide nose, skin darkening
    • mandibular prognathism (地包天 or 天包地)
  • arthralgia (joint stiff), bony and soft tissue overgrowth = sleep apnoea
  • headache, hypogonadal, microglossia (- size tongue)
166
Q

Complications for acromegaly?

A
  • cardiomegaly & hypertension
    • a very big risk factor!
  • increased risk of cerebrovascular events and headaches
  • MSK - bony / soft tissue overgrowth / arthritis
  • insulin resistant diabetes or exacerbation of type 2
  • sleep apnea
167
Q

Key investigations for acromegaly?

A

IGF-1 test

Glucose tolerance test

168
Q

Mechanism & diagnostic of growth hormone test for acromegaly

A

In normal patients, GH falls as glucose wears off, in acromegaly = opposite = GH peaks as glucose wears off

diagnostic if there is no suppression of glucose, since normally glucose should inhibit GH release

169
Q

Relevance of IGF-1 in acromegaly testing?

A

secreted by liver in response to growth hormones

almost always raised in acromegaly & fluctuate less than GH
this is diagnostic if high (if not → OGTT)

170
Q

How might you further assess / confirm acromegaly?

A

Glucose tolerance test (GTT)

Imaging - ECG / ECHO for cardio disease

check for pituitary adenoma

171
Q

How would you check for a pituitary adenoma?

A
  • visual field exam - can be bilateral temporal hemianopia due to pituitary adenoma
  • MRI scan of pituitary fossa
  • serum lactin will be raised if pituitary adenoma
172
Q

1st line treatment for acromegaly?

A
  • *pituitary surgery** - transsphenoidal
  • *remove tumour**, correct & prevent tumour compression of surrounding struc

difficult if large size & invasive, most needs lifelong monitoring

173
Q

if surgery fails, pharmacological therapy options for acromegaly?

A

dopamine agonists - cabergoline
fair amt wont respond

somatostatin analogues - IM octerotide or lanreotide
bound & inhibit multitude of hormones
SE GI cramps, flatulence, loose stools

growth hormone receptor antagonist - SC Pegvisomant
blocks IGF-I action, GH analogue

174
Q

Option besides surgery and pharma?

A

radiotherapy - lots of options

175
Q

What is prolactinoma?

A

excessive prolactin secretion by the lactotroph cell tumour of the pituitary

176
Q

What is prolactin?
secreted by? inhibited by?

A

secreted - anterior pit
tonic inhibited - dopamine
= if dopa stops, prolac will rise

function (and a rise leads to)
lactation
reduced sex hormones

177
Q

Hyperprolactin - besides prolactinoma,
can be caused by?

A

pituitary stalk damage

drugs - metoclopramid or ectasy

physiological - preggers, breastfeed, stress

178
Q

Presentation for prolactinoma?

A

menstrual dysfunction (often initial!), infertility, galactorrhoea, low libido, erectile dysfunc / low testosterone, reduced facial hair

tumour - headache, bitem hemia, CSF leak from skull base erosion

179
Q

Galactorrhoea can also be caused by

A

liver disease!! - associated with impaired oestrogen metabolism, which can cause breast tissue growth

Antipsychotics, antidepressants (SSRIs), Cimetidine, beta-blockers

180
Q

Investigation for hyperprolactimea?

A

blood test

for basal prolactin levels

181
Q

Differentials for hyperprolactimea

A

non functioning pituitary tumour - compression will interfere, but even then prolactin will be low

antidopaminergic drugs

macro / micro (<1cm) prolactinoma

182
Q

Management of prolactinoma?

A

Pharma only - use dopamine agonists
e.g. carbergoline, bromocriptine, quinagolide

usually remarkable shrinkage in a day/two

  • *macro** - usually sight change will improve!
  • *micro** - respond to carbergoline once / twice / week
183
Q

What is vasopressin?

A

= AVP = ADH Anti diuretic hormone

184
Q

Function of vasopressin?

A

act on collecting ducts by inserting aquaporin 2 channels therefore

allow kidney to reabsorp water → concentrates urine: increase H2O permeability in kidney, due to concentration gradient in the glomerular nephron

also causes vasoconstriction on vasculature = restore arterial BP

185
Q

Vasopressin - controls?
secreted by? controlled by?

A

made in paraventriculae nuclei in hypothalamus

secreted by posterior pituitary
(other one is oxytocin)

release controlled by

  • *osmoreceptors** in hypothalamus = d2d
  • *baroreceptors** in brainstem & great vessels = emergency
186
Q

What is diabetes insipidus?

A

passage of large volume (>3 L / day) of dilute urine due to impaired water reabsorption in the kidney either due to
lack of vasopressin secretion or vaso resistence

plasma osmolality will be high, urine osmolality will be low

187
Q

Differentiate cranial DI from nephrogenic DI?

A

Cranial = lack of vasopressin secretion, congenital defect in ADH gene

Nephrogenic = resistance to action of vasopressin by kidneys, acquired or congenital

188
Q

Causes of cranial DI?

A

tumour - never anterior pituitary though

severe head injury → damage to hypothalamus or pit gland

complications from neuro or pit surg

189
Q

Causes of Nephrogenic DI?

A

Congenital - AVPR2 or AQP2 mutations

Acquired - lithium (BPD), +Ca, -K, kidney infect

190
Q

Presentation DI?

A
  • *polyuria** = excessive urine, 15L in 24 hours
  • *hypernatraemia** = water loss > Na loss

polydipsia = excessive thirst

can dehydration

NO glycosuria

191
Q

How might you diagnose DI?

A

urine volume measure to confirm polyuria

Water deprivation then vasopressin test

(must be > 3L / day)

192
Q

Briefly outline the water deprivation test?

A

morning = osmolality measure, stop patient from drinking.

see if osmolality increases, if so is it matched in urinary osmolality?

  • normal individuals = urine concentration gets darker (higher) as no water
  • DI = osmolality not matched in urine, does not get concentrated
193
Q

How can the vasopressin test be used to differentiate between cranial and nephrogenic DI?

A

Give IM Synthetic vasopressin (= desmopressin) & water at 4pm
[vasopressin concentrates urine]

cranial = give both = plasma osmolality falls, urine osmolality increases (will be more concentrated)

nephrogenic = urine stays the same as resistant to vasopressin

194
Q

What is hypertonic saline infusion and measurement of vasopressin used for?

A

measures copeptin, a part of the same protein that vasopressin is made

able to distinguish primary polydipsia from two DI’s

195
Q

Management for cranial DI?

A

TUC

desmopressin - works at V2 receptor, maintain sodium and symptomatic relief

196
Q

Management for nephrogenic ID?

A

TUC, avoid precipitation drugs

free access to water, very high dose desmopressin

can try thiazide diuretics → encourage kidney Na+ uptake or NSAID - inhibit prostaglandin which locally inhibit action of ADH

197
Q

What is SIADH?

A

Syndrome of anti-diuretic hormone secretion

= continuous & excess secretion of vasopressin despite plasma being very dilute → hyponatraemia

= opposite of DI
urine osmolality will be high, plasma osmolality will be low

198
Q

Cause of SIADH?

A

Proton Pump Inhibitor!!!!!

Tumours - pituitary tumour, carcinoma of lung, other

Respiratory causes

199
Q

Signs and symptoms - SIADH

A

reduction in GCS and confusion with drowsiness, fits and coma - occurs later

water retention - lose salt in urine, can’t switch on urino angiotensin, no aldesterone
but clinically no oedema

increased GRF, less Na reabsorption in PCT

normal thyroid and adrenal func

200
Q

How might you distinguish SIADH from salt & water depletion?

A

test with 1-2l of 0.9% saline

SIADH will not respond, sodium depletion will respond!

201
Q

Treatment options for SIADH?

A

TUC, fluid restriction, U&E replacement

202
Q

If giving U&E, must be careful of?

A

Reperfusion injury - osmolality demyelination syndrome

can demyelinate the brain and irreversible (if chronic) - may take up to 2 weeks to manifest

LIMIT is <8 mmol / l whereas normal < 10-12 mmol/l in any 24 hour period

203
Q

Pharmacological options for SIADH?

A

Selective V2 receptor oral antagonist = tolvaptan

  • competitive antagonist to vasopressin
  • cause a profound ‘aquaresis’
    • collecting duct impervious to water, water is able to pass out

Salt and loop diuretic = furosemide to prevent circulatory overload

204
Q

Presentation thyroid cancer

A
  • Thyroid nodule/mass
  • Hoarseness/change in voice
  • difficulty swallowing & breathing
  • Cervical lymphadenopathy
  • Stridor (a harsh, high pitched sound, normally heard on inspiration, indicative of upper airway obstruction)
205
Q

Types of thyroid cancer and specific features

A

Thyroid follicular epithelial-derived cancer
FEMALE ELDERLY risk

Papillary - (commonest) younger, lymph node mets (separate from gland)

Follicullar- womenn

Anaplastic - 65 female high aggressive poor prog

Medullary = neuroendocrine, secretes calcitonin!
MEN II, RET gene

Primary thyroid lymphoma = with Hashimoto’s

206
Q

Free card for break

A
207
Q

Parathyroid hormone
released from?

A

by chief cells in four parathyroid glands in each corner of thyroid gland

208
Q

Parathyroid hormone
released in response to? controlled by?

A

low serum calcium

low magnesium and & high serum phosphate

controlled through negative feedback by serum sodium! (increase Ca = suppress)

209
Q

Where is does PTH act on and what is its function?

A

increase serum calcium to 1.1 mmol/l by

increasing activity of osteoclast
= reabsorption of Ca from bone

increasing calcium reabsorp in kidneys
in distal convoluted tubule
and in the GI tract

stimulate kidney to convert vitamin D3 to calcitrol = active form = promotes Ca absorption form food in small intestine

210
Q

Function of vitamin D in Ca physiology

A

converted by PTH to active form

act on all three of processes

therefore acts along PTH to increase Ca reabsorption

211
Q

Epidemiology of hyperparathyroidism?

A
  • esp in elderly women
  • primary hyperparathyroidism & malignancies = most common causes of hypercalcaemia
  • but hypercalcaemia is rarely the first presenting symptom of malignancy
212
Q

Types of hyperparathyroidism?

A

Primary

Secondary

Tertiary - as extension of secondary

213
Q

Outline pathophysio of primary hyperparathyroidism?

A

uncontrolled PTH production by tumour of parathyroid gland

80% due to single benign adenoma (out of 4 parathyroid), 15-20 due to gland hyperplasia, < 0.5% malignant

mostly asymptomatic. surgical removal

214
Q

Outline pathophysio of secondary parathyroidism?

A

insufficient vitamin D or chronic kidney disease = low Ca → compensatory PTH → hyperplasia / hypertrophy of gland

215
Q

Outline pathophysio of tertiary hyperthyroidism?

A

secondary continues for years

hyperplasia of gland after secondary, baseline PTH increases dramatically but long term ⇒ autonomous gland even after tx

surgical removal partial

216
Q

Disease pictures of the three types of hyperthyroidism?

A

Primary - high PTH, high Ca
normal phos / alk phos

**Secondary** - high PTH, low Ca
high phos (renal disease) / alk phos

Tertiary - high PTH, high/norm Ca

217
Q

What is malignancy hyperparathyroidism?

A

fake PTH secreted by carcinomas → mimic
= parathyroid related protein
squamous cell lung, breast, renal

so high Ca, normal PTH

calcium mobilisation, secondary mets in bone

218
Q

Signs and symptoms of hyperparathyroidism?

A

Bones, stones, groans and moans

  • Bones - from excessive bone resorption
    • pain & fractures
    • osteoporosis / osteopenia / osteomalacia
    • osteitis fibrosa cystica
  • Kidney stones - from excessive calcium = renal colic or biliary stone
  • Psychic moans
    • confusion, depression, anxiety, insomnia
  • Abdominal groans
    • abdo pain
    • constipation
    • acute pancreatitis
    • polyuria & nocturia - if ca2+ deposit in renal tubules
    • high ca2+ also dehydration, confusion and risk of cardiac arrest
219
Q

How would you investigate the parathyroid in hyperparathyroidism?

A
  • PTH measure
  • renal function measure - if low then secondary or tertiary?
    • Albumin-adjusted serum calcium
  • 24 hour urinary calcium
    • high in hypercalcaemia
    • where excess reabsorp despite hypercalcaemia, urinary will be low
220
Q

What imaging would you use for hyperparathyroidism

A
  • doppler ultrasound / CT / MRI - malignancy // radioisotope scanning will be 90% sensitive for adenomas
  • DXA bone scan - bone effects
221
Q

How would you treat hyperparathyroidism

A

primary & tertiary - surgery

secondary - TUC replace vit D or renal transplant in those with renal failure

222
Q

Pharmacological tx for hyperparathyroidism post surgery!

A
  • hypocalcaemia after surgery
  • if surgery CI = calcimimetic - increase sensitivity of parathyroid cells to ca2+ thereby causing less PTH secretion - e.g. oral cinacalcet
  • avoid thiazide diuretics and high ca2+ and vitamin D intake
223
Q

What is an acute severe hyperglycaemia & tx?

A

= emergency!

  • rehydrate IV 0.9% saline fluids to prevent stones
  • bisphosphonates after rehydration IV pamidronate to prevent bone resorption
  • measure serum UE and serum ca2+ 48hrs post tx
  • glucocorticoid steroids ORAL prednisolone in myeloma, sarcoidosis and vit D excess
224
Q

How might hypercalcaemia present?

A

rarely first sign of hyperparathyroidism! but

  • renal stones
  • ECG: short QT
  • thirst: polyuria (diluted)
  • nausea, constipation, confuse, coma
225
Q

Causes of hypercalcaemia?

A

malignancy - mets, PTH related peptides

primary hyperparathyroidism

226
Q

When looking at high / low Ca results, always question if ‘true’ or ‘pseudo’ - think these

A

tourniquet damage

sample is old and haemolysis

if low - hypoalbuminaemia?

227
Q

How would you correct calcium from albumin

A

(40 - serum albumin ) *0.02 + total serum calcium

for every gram that serum albumin is below 40, + 0.02

228
Q

Epidemiology of hypoparathyroidism?

A
  • all ages and both sexes
  • extremely common in hospitalised patients and correlates with severity of illness - in 88% of intensive care patients
229
Q

Causes of hypoparathyroidism?

A

secondary to increased serum phosphate
chronic kidney disease - most common cause

severe vitamin D deficiency
malabsorption, crohn’s, anti-epileptic drugs

reduced PTH function

230
Q

Define primary hypoparathyroidism?

A

= gland failure
PTH low, Ca+ is low, Phosphate high

autoimmune causes - DiGeorge or idiopathic

231
Q

Define secondary hypoparathyroidism

A

post- surgical or radiation

232
Q

Define secondary hypoparathyroidism

A

post- surgical or radiation

233
Q

Define functional hypoparathyroidism?

A

caused by Magnesium deficiency

  • present with low PTH & low Ca
  • need magnesium to excrete PTH! (carry vesicle to cell surface)
    • caused by alcoholic, drugs etc
234
Q

Presentation of hypocalcaemia?

A

SPASMODIC

Spasms - Trousseu’s sign (how much)

Periodical paraesthesia

Anxious, irritable, irrational

Seizures

Muscle tone +
wheeze + longer QT

Orientation impaired & confusion

Dermatitis

Impetigo herpetiformis - reduced Ca and pustules in preggers

Chvostek’s sign, Cataract, Cardiomyopathy

235
Q

What is the Trusseau’s sign?

A

sign of muscle spasm in the hands

inflate BP cuff to 20 mmhg above systolic for five minutes

positive if hand elicit ‘how much’ sign

236
Q

What is the Chvostek’s sign?

A

sign of muscle spasm

tap over facial nerve and twitch of facial muscles

sign of hypocalcaemia

237
Q

Define pseudohypoparathyroidism?

A

organs resistant to PTH
mutation in GNAS1 receptor

low Ca, high PTH

inherited from father

238
Q

Presentation pseudohypoparathyroidism

A
  • short stature, obesity, round facies, mild learning difficulties
  • subcutaneous calcification
  • !! short fourth metacarpals
    • make a fist & fourth metacarpal won’t be there → just a dimple
    • 4th and 5th may be same length
  • other hormone resistance
239
Q

Diagnostics for hypoparathyroidism?

A
  • usually history is enough
  • bloods
    • low serum calcium - used to confirm history
      • remember to correct for albumin abnormality
    • urea:creatinine for eGFR for renal disease
    • serum PTH
      • absent / low in hypo
      • high in other causes of hypocalcaemia
    • parathyroid antibodies - for idiopathic
    • serum 25-hydroxyvitamin D - low in vit D deficiency
    • Mg2+ level - severe hypomagnesaemia - functional hypoparathyroidism
240
Q

How would you treat hypoparathyroidism / hypocalcaemia generally?

A
  • calcitonin
    • decreases plasma Ca2+ and phosphate
  • bisphosphonates - reduce osteoclast activity therefore stop ca2+ declining
  • calcium supplements + calcitrol (active vit D)
241
Q

How would you treat an acute episode of hypocalcemia?

A
  • tetany
    • IV calcium gluconate over 30 min with ECG monitoring
  • vitamin D deficiency
    • oral colecalciferol (D3) or oral Adcal (calcium + D3) (calcitrol?)
    • ineffective for those with hypoparathyroidism as PTH is needed to convert D3 to 1, 25 dihydroxyvitaminD
242
Q

Aldosterone is secreted by?

A

Zona glomerulosa of the adrenal gland

243
Q

Aldosterone is a part of which system?

A

Renin-angiotensin-aldosterone
increases BP

244
Q

Briefly outline the renin-angiotensin-aldosterone system?

A

renin (kidney) on angiotensinogen (liver) → angio I → ACE → angio II → stimulates release of aldosterone

raises BP by both angiotensin II & aldosterone

245
Q

What cells monitors the BP in kidneys
& where is it located?

A

juxtaglomerular cells
monitors kidney BP

in the afferent arteriole

246
Q

Aldosterone acts on which part of the body and what effects does it have?

A

on the distal tubules

  • *sodium reabsorption**
  • *potassium secretion**

on the collecting ducts
hydrogren secretion

247
Q

Nature of aldosterone?

A

Minerocorticoid steroid hormone

248
Q

Overall effects of aldosterone?

A

increase sodium reabsorption into blood
= water also reabsorped (retain H2O)

blood volume is increased, systemic vascular resistance changed,
blood pressure is increased

249
Q

Biggest linked condition with hyperaldosteronism?

A

most common cause of secondary hypertension

consider hyperaldosteronism if patient not responding to hypertension treatments!

→ screen with renin aldosterone ratio blood test, clue can be low potassium in blood

250
Q

Presentation for hyperaldosteronism?

A

hypertension &

hypokalaemia (often absent)
but may present as:

  • muscle weakness, paraesthesia, mood disturbance
  • polyuria / nocturia as potential diuresis
251
Q

What is Primary hyperaldosteronism

A

= Conn’s syndrome

= when adrenal glands secretes too much aldosterone

= serum renin is low (renin is only secreted when BP is high!) → suppressed by high BP entering kidneys

252
Q

Causes of primary hyperaldosteronism?

A

adrenal adenoma = 30-40%

bilateral adrenal hyperplasia = 60-70%

familial hyperaldosteronism

adrenal carcinoma (rare)

253
Q

What is secondary hyperaldosteronism?

A

= when excessive renin is stimulating the adrenal gland to produce more aldosterone

= serum renin will be high → cause!

254
Q

Causes of secondary hyperaldosteronism?

A

principle = juxtaglomerular cells, which senses kidney BP, keep sensing low → lots of renin → adrenal stimulated but kidney will not feel high BP

renal artery stenosis
= narrowing of artery supplying the kidney
= atherosclerosis (plaque)

renal artery obstruction

255
Q

How would you confirm hyperaldosteronism & differentiate?

A

renin : aldosterone ratio in blood

low / normal renin = primary
high renin = secondary

256
Q

How would you investigate for causes of hyperaldosteronism?

A

Imaging

CT / MRI
for adrenal tumour

Renal doppler ultrasound, CT angiogram or MRA
for renal artery stenosis or obstruction

257
Q

3 classic investigative findings for hyperaldosteronism?

A

BP - hypertension

Serum electrolytes - hypokalaemia

Blood gas - alkalosis

258
Q

What is hyperaldosteronism typically associated with?

A

Heart failure

259
Q

How would you pharmacologically manage hyperaldosteronism?

A

aldosterone receptor antagonists

  • eplerenone - no gynaecomastia
  • spironolactone - gynaecomastia
  • if not tolerated - ENaC inhibitor = amiloride

antihypertensives if needed

260
Q

Which aldosterone receptor antagonist could potentially cause gynaecomastia?

A

spinocolactone

261
Q

How would you surgically treat hyperaldosteronism?

A

surgically remove adrenal adenoma

percutaneous angioplasty for renal artery stenosis

262
Q

What is adrenal insufficiency?

A

= adrenal glands do not produce enough steroid hormones, particularly cortisol & aldosterone.

primary = Addison’s

263
Q

Briefly outline the adrenal axis?

A

Hypothalamus = CRH
Corticotrophin releasing hormone

Anterior pituitary = ACTH
adrenocorticotrophic hormone

Adrenal gland = cortisol

Cortisol inhibits CRH & ACTH throgh negative feedback

264
Q

Function of cortisol?

A

= major metabolic & stress hormone

  • inhibits immune system & bone formation
  • raises blood glucose
  • increases alertness & metabolism
265
Q

Key signs of adrenal insufficiency!

A

= bronze hyperpigmentation to skin
particularly in skin creases like hands

  • *= hypotension,** particularly
  • *postural hypotension**

= low Na, high potassium
hyponatraemia, hyperkalaemia

266
Q

Symptoms of adrenal insufficiency?

A

HYPOTENSION, low Na high K

  • dehydration
  • reduced libido, hair loss in axilla / pubic region !! esp in women
  • weight loss, muscle wasting
  • mood disturbance
  • cramps, abdo pain, fatigue, nausea, vomit
267
Q

What is primary adrenal insufficiency?

A

= Addison’s disease

= damage of the adrenal glands, resulting in a reduction of cortisol & aldosterone secretion

= high ACTH, trying to stimulate but no response or neg feedback (no cortisol production)

268
Q

What are the causes of primary adrenal insufficiency?

A
  • most common = autoimmune → esp in women
  • infective
    • tuberculosis (most common worldwide)
    • HIV, fungal, syphilis
  • other
    • haemorrhage
    • malignancy
269
Q

What is secondary adrenal insufficiency?

A

= inadequate (low) ACTH stimulating the adrenal glands

270
Q

Causes of secondary adrenal insufficiency?

A
  • loss or damage to the pituitary gland
    • injury, surgery, radiotherapy
    • infection
    • loss of blood flow
  • pituitary gland necrosis from massive blood loss during childbirth - Sheehan’s syndrome
271
Q

What is tertiary adrenal insufficiency?

A

= inadequate CRH release by hypothalamus

272
Q

Causes of adrenal insufficiency?

A

= steroids not being tapered off properly

long term exogenous steroid being suddenly withdrawn, hypothalamus doesn’t wake up fast enough & no replacement

= taper slowly for adrenal axis to regain normal function

273
Q

How might you investigate adrenal insufficiency?

A

Short Synacthen = test of choice!

Plasma ACTH = primary / secondary

adrenal autoantibodies
= adrenal cortex antibodies & 21 hydroxylase antibodies

Imaging if suspecting tumour, haemorr or other structural pathology

274
Q

How might plasma ACTH differentiate between primary & secondary adrenal insufficiency?

A

primary = high ACTH
trying to get adrenal to work

secondary = low ACTH
loss of injury to pit

275
Q

What are the autoantibodies associated with Addison’s?

A

adrenal cortex antibodies & 21 hydroxylase antibodies

276
Q

Outline the short synacthen test?

A

give synacthen = synthetic ACTH
(IV 250 mcg of tetracosactide)
in the morning

measure blood cortisol at baseline, 30 & 60 minutes after administration

277
Q

How might you interpret the results of the short synacthen test?

A

if blood cortisol

double of baseline = pituitary issue
(secondary) as adrenals responsive

less than double of baseline = adrenal issue
(primary) = Addison’s as not responsive

278
Q

How might you treat someone with adrenal crisis?

A

= replacement steroids titrated to signs, symptoms and electrolytes

hydrocortisone for cortisol

fludrocortisone for aldosterone

steroid card and tag, double dose in acute illness

279
Q

What is an Addisonian crisis?

A

= adrenal crisis, acute Addison’s
emergency

can be first presentation of Addisons

or triggered by infection, trauma, or other acute illness in someone with est. Addie’s or steroid withdrawal!

280
Q

Presentation of an acute adrenal crisis?

A

HYPOtension

low glucose, low Na, high K

reduced consciousness, patient very unwell

281
Q

How might you treat an acute adrenal crisis?

A

parenteral steroids - IV hydrocortisone 100mg stat then 100mg every 6 hours

  • IV fluid resus
  • correct hypoglycaemia
  • careful monitoring of electrolytes and fluid balance
282
Q

What is serotonin syndrome?

A

due to increased serotonergic activity in CNS which can be induced by a range of medications that increase serotonergic transmission by altering neurotransmitter serotonin

283
Q

Risk factors of serotonin syndrome?

A

within several hours of taking a new drug

increasing the dose of a drug you’re already taking

Overdose

in all ages, esp young adults

284
Q

Function of serotonin?

A

= monoamine neurotransmitter derived from tryptophan

CNS = theromoregulation, behavior, attention

PNS - vasoconstriction, bronchoconstriction, GI motility, uterine contraction

Promotes platelet aggregation = risk
haemorrhagic + if used with antiplatelet

285
Q

Drugs implicated in serotonin syndrome?

A

serotonin inhibitors, receptor agonists,
impaired serotonin reuptakes, increased

SSRI’s, SNRI’s. TCA, MAOI

MDMA (ectasy), cocaine, lithium!

286
Q

Outline pathophysiology of SS?

A

serotonin reuptake is inhibited from synaptic cleft into presynaptic neuron

287
Q

Presentation of serotonin syndrome?

A
  • altered mental status
    • anxiety, restless, disorientation, or agitation
  • autonomic hyperactivity = HYPER tension, thermia, TACHYCARDIA
    • flushed skin, diaphoresis (sweating lol)
  • neuromuscular abnormalities
    • dilated pupils
    • clonus (repeat rhythmic), myoclonus (sudden)
    • positive babinski! bilateral upgoing plantars
288
Q

How might you investigate serotonin syndrome?

A

Hunter criteria

patient is taking a serotonergic agent and presents with ONE of the following

spontaneous clonus
Inducible/ocular clonus and agitation or diaphoresis
tremor / hyperreflexia
hyperthermia, hypertonia, ocular / inducible clonus

289
Q

differentials for serotonin syndrome?

A

MDMA / cocaine use

neuroleptic malignant syndrome

broad as it is with confusion - encephalitis, drug intox, phaechromocytoma

290
Q

What is the general tx for serotonin syndrome?

A

observation, supportive care if needed

cardiac monitoring, electrolyte, acute kidney, rhabdomyolysis

iv fluids, antipyretics

specific antihypertensive for profound hypertension

291
Q

Specific antihypertensive for serotonin syndrome?

A

cyproheptadine, and propofol

292
Q

Mechanism of cyproheptadine

A

histamine receptor antagonist with action against serotonin receptors

293
Q

Complications of serotonin syndrome?

A
  • Cardiac arrest
  • Cardiac arrhythmias
  • Acute kidney injury
  • Rhabdomyolysis
  • Disseminated intravascular coagulation
  • Seizures
  • Respiratory failure
  • Venous thromboembolism
294
Q

What is rhabdomyolysis?

A

clinical syndrome characterised by skeletal muscle necrosis due to release of toxic intracellular contents including myoglobin and electrolytes

295
Q

Aetiology of rhadomyolysis?

A

(3)

Muscle compression from crush injury
compartment syndrome, surgical operation, electrical injury, prolonged immbo

Non traumatic, exertional

Non traumatic, non exertional
statins & colchicine, cocaine, opioids, benzodiazepines, amphetamine, toxins

296
Q

What leaks out of the muscles during rhabdomyolysis?

A

creatinine kinase and myoglobin

297
Q

High risk of which disease is linked to rhabdomyolysis?

A

AKI as creatinine kinase inceases

298
Q

Pathophysio of rhabdomyolysis

A

myocyte injury
= as a cause or as a step in process
depletes ATP = everything foes

releases creatinine kinase & myoglobin

myocyte damages kidney - renal rubular obstruct, intrarenal vasoconstrict

creatinine also increase risk of AKI

299
Q

Rhabdomylysis presentation & trigger?

A

suspect when unexplained AKI = following immobile, crush, muscle tender or meh U&E

myalgia, muscle weakness, dark urine (coca cola)
aches, calves & lower, from myoglobin

others - soft tissue swelling, altered mental status // skin changes, limb deformity

300
Q

investigations for serum creatine kinase?

A

serum creatine kinase - KEY
= marker of skeletal breakdown
= rhabdo if CK > 5x upper limit of normal
will rise within 12 hrs of injure & peak 24-72

Myoglobin in urine
= 50% patients as excreted quickly
= will show on dipstick as ‘blood’

Renal function - stat!
= 15-50% will have AKI
= risk increases with higher CK

ECG = risk of UE abnormality

301
Q

Management for rhabdo?

A

fluid resus aggressive and early

dialysis if needed

loop diuretics, IV bicarb

302
Q

What is carcinoid syndrome

A

syndrome which arise when a neuroendocrine tumour (aka carcinoid syndrome) begins secreting hormones

303
Q

What is a carcinoid tumour?

A

Tumour of the neuroendocrine cells

releases hormones into blood
e.g. serotonin, histamine, bradykinin (vdilate), prostaglandins (vdilate)

304
Q

When do symptoms usually arise?

A

when tumour has spread to the liver** and releasing hormones e.g. **serotonin into bloodstream

305
Q

Symptoms of carcinoid syndrome?

A

abdo - RUQ, diarr, const, poo blood
cough - blood, wheeze, short breath, pain
general cancer stuff

flushing of the skin! particularly the face bluish red - caused by bradykinin

fast heart rate, breathlessness, wheezing, carcinoid heart disease - heart valve thicken and stop working properly

306
Q

What is a carcinoid crisis?

A

when tumour outgrows its blood supply or is handled too much during surgery - mediators flow out

vasodilate, bronchoconstrict = bradykinin

tachycardia = serotonin

hypotension = ACTH

hyperglycaemia = glucagon and ACTH

exacerbated by alcohol and stress!!

307
Q

How might you diagnose a carcinoid tumour?

A

urinalysis = will show
increased 5 hydroxyindoleacetic acid

imaging = ct, mri scan
otreoscan / gallium 68 pet scan

blood test = niacin deficiency!

308
Q

How might you treat carcinoid syndrome?

A

surgical removal of tumor

pharmacology

lifestyle - avoid ALCOHOL & stress
as symptoms exacerbated

309
Q

Surgical options to remove carcinoid tumor?

A

removal, radiotherapy,

block blood supply to the tumour esp if in liver = hepatic artery embolisation

310
Q

pharmacological options to treat carcinoid tumor?

A

somatostatin analogues

= octreotide and lanreotide - slows growth of the tumour, receptor antagonist

311
Q

Lifestyle advice for carcinoid syndrome?

A

avoid alcohol and stress

avoid food with tyramine = in aged cheese, salted or pickled meats,

avoid spicy food

312
Q

What is a pheochromocytoma?

A

tumour of the chromaffin cells in adrenal glands which secretes unregulated and excessive amounts of adrenaline

313
Q

What is phaeochromocytoma linked to?

A

Linked to multiple endocrine neoplasia type 2 (MEN2)!!, Von Hippel Lindae syndrome

314
Q

Adrenaline is secreted by?

A

Chromaffin cells in adrenal medulla of adrenal glands

315
Q

Effects of the tumour?

A
  • alpha-adrenergic - + BP, increased cardiac contract, increased glycogenolysis / gluconeogenesis (glucose utilise)
  • beta-adrenergic - increased heart rate and contractility
316
Q

Where might you find a phaeochromocytoma?

A

abdomen >95%

317
Q

Symptoms of a phaeochromocytoma?

A

PAROXYSMAL

episodic headache

sweating

tachycardia, palpitations, paroxysmal atrial fibrillation
→ resembles panic attack

318
Q

What is a phaeochromocytoma crisis?

A

= hypertensive crisis, if severe could lead to circulatory collapse

= hypertension, hyperthermia, confusion
end organ dysfunction - cardiomyopathy, pulmonary oedema

319
Q

How might you diagnose phaeochromocytoma?

A

24 hour urine catecholamines

plasma free metanephrines
= breakdown product of adrenaline

CT / MRI cross section
alt MIBG scintigraphy - MIBG substance taken up by adrenergic tissue

320
Q

How might you manage a phaeochromocytoma?

A

BP control
= phenoxybenzamine, alpha blocker
irreversible, long acting

alt CCB, and beta blocker once established on alpha blockers

Metyrosine - inhibit catecholamine synthesis

High sodium diet to replace with excessive catecholamines

adrenalectomy = removes the tumour = GOLD

Phase 2A (12 decks)

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